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Brain-derived tau oligomer polymorphs: distinct aggregations, stability profiles, and biological activities.
Commun Biol
January 2025
Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Aggregation of microtubule-associated tau protein is a distinct hallmark of several neurodegenerative disorders such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and progressive supranuclear palsy (PSP). Tau oligomers are suggested to be the primary neurotoxic species that initiate aggregation and propagate prion-like structures. Furthermore, different diseases are shown to have distinct structural characteristics of aggregated tau, denoted as polymorphs.
View Article and Find Full Text PDFSocial Vulnerability and Biological Aging in New York City: An Electronic Health Records-Based Study.
J Urban Health
January 2025
Department of Environmental Medicine and Climate Science, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Place, Box 1057, New York, NY, 10029, USA.
Chronological age is not an accurate predictor of morbidity and mortality risk, as individuals' aging processes are diverse. Phenotypic age acceleration (PhenoAgeAccel) is a validated biological age measure incorporating chronological age and biomarkers from blood samples commonly used in clinical practice that can better reflect aging-related morbidity and mortality risk. The heterogeneity of age-related decline is not random, as environmental exposures can promote or impede healthy aging.
View Article and Find Full Text PDFMyelin debris as an initiator of microglial dysfunction and neuropathology in Alzheimer's disease.
Cell Mol Immunol
January 2025
Center for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia (UVA), Charlottesville, VA, 22908, USA.
Dynamic switching between brain networks predicts creative ability.
Commun Biol
January 2025
Department of Psychology, Pennsylvania State University, University Park, Pennsylvania, USA.
Creativity is hypothesized to arise from a mental state which balances spontaneous thought and cognitive control, corresponding to functional connectivity between the brain's Default Mode (DMN) and Executive Control (ECN) Networks. Here, we conduct a large-scale, multi-center examination of this hypothesis. Employing a meta-analytic network neuroscience approach, we analyze resting-state fMRI and creative task performance across 10 independent samples from Austria, Canada, China, Japan, and the United States (N = 2433)-constituting the largest and most ethnically diverse creativity neuroscience study to date.
View Article and Find Full Text PDFThe TRPV1-PKM2-SREBP1 axis maintains microglial lipid homeostasis in Alzheimer's disease.
Cell Death Dis
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Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Microglia are progressively activated by inflammation and exhibit phagocytic dysfunction in the pathogenesis of neurodegenerative diseases. Lipid-droplet-accumulating microglia were identified in the aging mouse and human brain; however, little is known about the formation and role of lipid droplets in microglial neuroinflammation of Alzheimer's disease (AD). Here, we report a striking buildup of lipid droplets accumulation in microglia in the 3xTg mouse brain.
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